Abstract
Granulomatous infection caused by the dimorphic fungus, Histoplasma capsulatum var. capsulatum. Worldwide distribution with prevalence in the Mississippi and Ohio River Valleys in the United States.
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Keywords
Overview
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Granulomatous infection caused by the dimorphic fungus, Histoplasma capsulatum var. capsulatum
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Worldwide distribution with prevalence in the Mississippi and Ohio River Valleys in the United States
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Found in soil and vegetal detritus contaminated by bird and bat droppings with acquisition via aerosol inhalation or less commonly via direct innoculation
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Risk factors include immunocompromised host and occupations with exposure to high risk environments
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Immunocompromised individuals are more likely to develop disseminated disease to various extrapulmonary locations (e.g. liver, spleen, lymph nodes, bone marrow, skin, CNS, adrenal glands)
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Fever, malaise, loss of appetite and fatigue are common nonspecific presenting symptoms
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Cutaneous involvement is uncommon (~5% of cases, may be higher in severely immunosuppressed hosts) but is a helpful diagnostic clue when present
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Clinical Presentation
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In the majority of cases the infection is asymptomatic or mild with a self-limited course
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Characterized by three different forms––namely pulmonary, primary cutaneous, and disseminated disease, the latter of which is severe
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Primary cutaneous histoplasmosis due to direct inoculation is uncommon and presents as an isolated ulcer with regional lymphadenopathy that self-resolves
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Secondary cutaneous histoplasmosis seen in disseminated disease is due to hematogenous spread and is characterized by diverse skin morphology including papules, plaques, nodules, umbilicated papules, acneiform, abscess, cellulitis, pyoderma gangrenosum-like lesions or painful mucocutaneous ulcers (Fig. 40.1)
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Areas of involvement include the face, extremities, trunk, and mucosa (especially oral)
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Depending on organ involvement in disseminated disease symptomatology will vary but may include: petechiae, easy bruising, fatigue, weakness (thrombocytopenia and anemia from bone marrow involvement), hepatomegaly, splenomegaly, lymphadenopathy, altered mental status, photophobia, headache (CNS involvement)
Histopathology
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A varying degree of inflammation is seen characterized by a granulomatous, lymphocytic and/or a mononuclear infiltrate (Fig. 40.2)
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Yeast forms are 2–4 microns in size, often elongated, may demonstrate narrow budding, can have a peripheral rim of clearing
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Organisms are often parasitized by macrophages
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Yeast forms are highlighted by periodic acid-Schiff (PAS), Gomori-Grocott, or silver methenamine (GMS) stains
Differential Diagnosis
In all cases, travel history and exposure history is essential in narrowing the diagnosis; pathologic findings are often diagnostic and biopsy should be considered if any of these entities are suspected.
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Blastomycosis : may see larger lesions with a raised, crusted border with or without ulceration
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Coccidioidomycosis : there may be clinical overlap, but pathology is different and diagnostic
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Cryptococcosis : may have varied clinical presentations and can overlap with histoplasmosis skin findings; biopsy, culture, and serologic testing are helpful
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Paracoccidioidomycosis : lesions may be larger crusted nodules, but biopsy is diagnostic
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Leishmaniasis : bite-site crusted ulcers, which may be grouped, and frequently involve the ear can be helpful; be cautious with pathology as both leish and histo can look similar
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Tuberculosis : can be varied depending on if primary cutaneous involvement or a tuberculid response; pathologic findings are diagnostic
Work-Up
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A thorough history and physical exam should be obtained including evaluation of mucosal sites (oral and perianal)
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Histopathologic evaluation of a punch biopsy from a representative skin lesion should be performed
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Culture is considered the gold standard with an incubation time of 3–6 weeks
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Antigen testing of urine, serum, bronchial lavage or CSF is sensitive for acute disseminated and pulmonary histoplamsosis, but there is cross-reactivity with Paracoccidioides and Blastomyces
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Hypercalcemia has been described, which may be nonspecific (present in many granulomatous diseases)
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Evaluation for disseminated disease should be targeted based on potential organs of involvement
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CBC: leukopenia, thrombocytopenia, anemia (bone marrow/spleen involvement)
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Peripheral blood smear review to visualize the organism (Wright’s stain)
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CMP: abnormal AST, ALT, bilirubin
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Chest x-ray: typically will show diffuse interstitial or reticulonodular pulmonary infiltrates
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Abdominal CT (assess for enlarged liver, spleen, lymph node)
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Brain CT/MRI, lumbar puncture (CNS involvement)
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Endoscopy: Visualize GI lesions
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Treatment
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Treatment choice is based on disease severity and underlying comorbidities
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Amphotericin B is the agent of choice for induction therapy for severe disease
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Itraconazole is preferred for mild to moderate disease and is commonly used for maintenance therapy
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If conventional treatment fails additional options include voriconazole or posaconazole
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Patients with HIV/AIDS may require additional management and infectious disease experts should be consulted
Suggested Readings
Chang P, Rodas C. Skin lesions in histoplasmosis. Clin Dermatol. 2012;30(6):592–8.
Fernandez-Flores A, Saeb-Lima M, Arenas-Guzman R. Morphological findings of deep cutaneous fungal infections. Am J Dermatopathol. 2014;36(7):531–53.
Gupta V, Singhal V, Singh MK, Xess I, Ramam M. Disseminated histoplasmosis with hypercalcemia. J Am Acad Dermatol. 2013;69(5):e250–1.
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Ferguson, N.N. (2018). Histoplasmosis. In: Rosenbach, M., Wanat, K., Micheletti, R., Taylor, L. (eds) Inpatient Dermatology. Springer, Cham. https://doi.org/10.1007/978-3-319-18449-4_40
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